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Effects of an adrenal ll‐beta, 17‐alpha hydroxylase inhibitor in juvenile‐onset diabetes mellitus
Author(s) -
Narduzzi J. V.,
Sabeh G.,
Weir T. F.,
Cleary W. J.,
Danowski T. S.
Publication year - 1967
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt196785684
Subject(s) - endocrinology , medicine , diabetes mellitus , basal (medicine) , urinary system , beta (programming language) , alpha (finance) , ingestion , surgery , construct validity , computer science , patient satisfaction , programming language
An antiadrenal compound, 2‐{p‐aminophenyl)‐2‐phenylethylamine, which inhibited adrenocortical 17‐alpha and ll‐beta hydroxylase activity in animals, was administered for 3 week periods to 10 patients with diabetes of juvenile onset in an attempt to ameliorate the severity of the diabetes and was given for a lesser period to one patient with spontaneous Cushing's syndrome. The drug did not alter the intensity of the diabetes but it produced a partial remission of the Cushing's syndrome. In diabetes, ingestion of the dl form increased urinary 17‐ketosteroids, Porter‐Silber chromogens, and ll‐desoxycortisol metabolites in 3 and possibly 4 of 5 patients. This was observed only once in 4 trials with the d form. This suggests that the 1 form is more effective than the d form in inhibiting ll‐beta hydroxylase. Inhibition of 17‐alpha hydroxylase by the d form was either minimal or absent judging from the urinary levels of Porter‐Silber chromogens and ll‐desoxycortisol metabolites. In diabetes neither the d nor the dl preparation affected the basal plasma 17‐hydroxycorticosteroids nor the rise in this index which followed upon intravenous injection of ACTH. The basal plasma 17‐hydroxycorticosteroids were markedly lowered in Cushing's syndrome.